The high incidences of traumatic brain injury (TBI) in both the civilian and military population, and the absence of any prophylactic treatment for acquired epilepsy, such as posttraumatic epilepsy (PTE), create an urgent need to develop broad-spectrum and easily deployable therapeutic strategies. There are currently no ways to prevent the onset of posttraumatic epilepsy (PTE) following head injury. The administration of anticonvulsants after head injury may decrease early post traumatic seizures but has failed to impact the development of long-term epilepsy or improve the incidence of disability or death. Therefore, novel treatment paradigms are needed.
Several in vitro and in vivo studies have demonstrated that brain cooling by 10-20° C. reduces epileptiform activity in seizure models and in humans. Technologies based on cranially-implanted Peltier (thermoelectric) cells powered by batteries are under development to achieve such a high degree of cooling in the brain. However, clinical trials conducted to evaluate hypothermic antiepileptogenesis and neuroprotection have all failed. These clinical trials, which employed whole body cooling by ≧5° C. for a few days post-injury, failed to demonstrate effective treatment and were plagued by side effects, ranging from irregular heartbeat to kidney failure, due to the low body temperature.
The process of epileptogenesis in humans is not known. It is theorized that agents that are neuroprotective may also be antiepileptogenic, but no data is available to demonstrate this. Similarly, the process of ictogenesis (i.e., the precipitation of seizures) is not necessarily the same as epileptogenesis. It is therefore entirely possible that treatments that prevent the precipitation of seizures do not prevent the genesis of epilepsy and, vice versa, those that may prevent the onset of epilepsy may not be capable of shutting down existing seizures.
There are known devices that use active cooling to shut down epileptic seizures (antiepileptic effect). Known devices are based on the assumption that cooling a targeted area of the brain by about 10° C. is necessary to shut down the epileptic focus. Once such device is based on active Peltier cells that cool the brain, including heat pipes to cool deep into the brain. A second exemplary known device uses circulating coolant in tubing implanted within the dorsal hippocampus of a brain to achieve cooling of at least 7° C. in the hippocampus. Unfortunately, such devices are typically highly intrusive (if inserted deep into the brain) and require complex structures (e.g., heat pipes), electronics (Peltier elements), and long-lasting powering elements (e.g., batteries) to produce the necessary cooling. None of the known methods and devices provide continuous prevention of epilepsy (epileptogenesis), but only provide remedial action when a seizure begins so as to lessen the severity of the seizure.
What is desired, therefore, is an improved device for preventing and/or treating acquired epilepsy.